无症状性脑梗死患者血清炎性因子和纤溶及抗纤溶活性的变化

Changes of serum inflammatory cytokine, fibrinolytic and antifibrinolytic activities in patients with SCI

目的观察无症状性脑梗死(silent cerebral infarction,SCI)患者血清炎性因子和纤溶及抗纤溶活性的变化。方法选择SCI患者53例(SCI组)和健康体检者55例(对照组),分别检测血清高敏C反应蛋白(hs-CRP)、血浆纤溶酶原活性(PLG:A)、纤溶酶活性(PLM:A)、组织型纤溶酶原激活物(t-PA)活性、D-二聚体(D-D)含量、_2α-纤溶酶抑制剂(α_2-PI)和纤溶酶原激活物抑制剂(PAI)活性。结果 SCI组hs-CRP水平明显高于对照组[(15.36±4.30)mg/L vs (10.26±2.61)mg/L,P<0.01],SCI组PLM:A、t-PA和D-D含量均明显低于对照组[(35.84±10.23)% vs (68.74±18.41)%,(0.11±0.01)U/ml vs (0.49±0.12)U/mL(0.36±0.14)mg/L vs (0.68±0.16)mg/L,P<0.01)],SCI组PLG:A与对照组比较差异无统计学意义(P>0.05),SCI组α_2-PI活性和PAI活性明显高于对照组[(128.46±23.75)% vs (96.36±19.34)%,(0.86±0.22)AU/ml vs (0.48±0.10)AU/ml.P<0.01]。结论炎症过程和纤溶及抗纤溶系统的功能失调与SCl的形成有关。

Objective To observe the changes of serum inflammatory cytokine,fibrinolytic and antifibrinolytie activities in patients with silent cerebral infarction（SCI）. Methods The serum level of high-sensitivity C-reactive protein（hs-CRP） was measured by immunodiffusion turbidimetry in 53 patients with SCI and 55 cases of control group. The plasminogen activity（PLG ： A）,plasmin activity（PLM ： A）, tissue-type plasminogen activator （t-PA） activity, D-direct （D-D）, α2-plasmin inhibitor（α2-PI） activity and plasminogen activator inhibitor（PAl） activity were also measured in both groups. Results The level of hs-CRP was significantly higher in patients with SCI than in the control group [ （15. 36±4. 30） mg/L vs （10. 26±2. 61） mg/L, P 〈 0. 01]. The levels of PLM ： A,t-PA and D-D were markedly lower in SCI group than in the control group [（35.84± 10.23）% vs （68.74±18.41） %,（0.11 ±0.01） U/ml vs （0.49±0.12） U/ml,and（0. 36±0.14） mg/L vs （0.68 ± 0.16） mg/L, P 〈 0.01, respectively ], but PLG ： A was not significantly different between the two groups （P 〉 0.05）. The α2-PI activity and PAl activity were significantly higher in SCI group than in the control group[（128.46±23.75）% vs （96.36±19.34）%, （0.86± 0. 22） AU/ml vs （0. 48 ±0. 10） AU/ml, P 〈 0. 01, respectively]. Conclusion Inflammatory processes and dysfunction of fibrinolytic and antifibrinolytic systems are involved in the pathogenesis of SCI.